The long term patency of grafts or endarterectomy sites can be improved in medium and small caliber vessels by two general approaches: 1) modification of graft design and its thrombogenicity or 2) alteration of the coagulation system. Although morphologic and in vitro studies have emphasized the importance of the platelet and fibrin components of the coagulation system in graft healing, such studies necessitate either sacrifice of the graft or lack specificity for platelet-fibrin dynamics at the graft interface. To study platelet-fibrin kinetics directly and in vivo at the graft site, we propose to employ two new radio-nuclide probes: 111 In-labeled platelets and l3l I-labeled fibrinogen. In addition, selective histochemical, scanning electron microscopy and conventional histologic studies will correlate coagulation kinetics with known morphologic events in graft healing. Both the similarity of the baboon's coagulation system to man and the use of conventional graft materials will closely simulate the clinical situation. Following establishment of the "normal" dynamics of platelet and fibrin in the healing process, agents which are known to modify their activity such as ASA, dipyridamole, rheomacrodex and heparin will be employed in the same model. These studies have two potential clinical benefits: 1) improved patency in small caliber vessels by the rational selection of pharmacologic agents, and 2) the development of a mehtod of in vivo assessment of platelet-fibrin deposition. This latter technique may be applied not only to the healing of synthetic grafts, but also to ulcerative plaques, transplant rejection phenomena, neoplastic metastases - all of which appear related to this fibrin-platelet interaction.